Basal gastric acid secretion in nonulcer dyspepsia with or without duodenitis

Collen, Martin J.; Loebenberg, Michael J.

doi:10.1007/bf01536059

Cited by 73 publications

(33 citation statements)

References 13 publications

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“…This has been, however, an inconsistent finding in different clinical studies [1]. In general, basal gastric acid secretion in patients with functional dyspepsia has been reported to be similar to that in asymptomatic controls but significantly lower than that in patients with duodenal ulcer [2,3]. Similar results have been found with regard to stimulated gastric acid secretion [3].…”

Section: Targeting the Abnormalities Of Gastric Acid Secretionsupporting

confidence: 70%

Targeting the Abnormalities of Gastroduodenal Functions in Functional Dyspepsia

2001

Dig Dis

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The current definition of functional dyspepsia changes the previous concept of absence of organic disease to the presence of a functional alteration of the upper gastrointestinal tract. From a theoretical point of view, the alteration of any major gastrointestinal function may induce dyspeptic symptoms. However, both asymptomatic subjects with some gastrointestinal functional alteration and dyspeptic patients without a demonstrable dysfunction are not unusual. This may be explained at least in part by the more recent concept of visceral sensitivity. The potential role of acid secretion in the pathogenesis of functional dyspepsia as well as the positive effect of antisecretory drugs in a proportion of patients may be based on an increased gastric acid secretion and duodenal acid overload, a hypersensitivity to acid and/or the development of acid-mediated gastrointestinal motor abnormalities. Helicobacter pylori infection may play a role in this context. Both interdigestive and postprandial gastrointestinal motility, mainly a delayed gastric emptying and an altered intragastric distribution of nutrients, have been described to be disturbed in up to half of the patients with functional dyspepsia. This may also be an explanation for the high frequency of intestinal bacterial overgrowth in these patients. Most probably, visceral hypersensitivity should be present for motor alterations to induce symptoms. This is the basis for future development of new drugs in the management of this functional syndrome. The role of H. pylori in the pathogenesis of functional dyspepsia is a matter of discussion, but a proportion of patients benefit from eradication therapy and, therefore this therapeutic approach should be taken into account.

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Section: Targeting the Abnormalities Of Gastric Acid Secretionsupporting

confidence: 70%

Targeting the Abnormalities of Gastroduodenal Functions in Functional Dyspepsia

2001

Dig Dis

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“…Although we did not quantify gastric acid secretion, exaggerated gastric acid secretion seems less likely. Previous studies have shown normal gastric acid secretion in FD patients (25,26), and we excluded patients with recent use of acid suppressive drugs to avoid rebound acid hypersecretion (27,28). H. pylori infection may increase gastric acid secretion, but all our patients were H. pylori negative.…”

Section: Discussionmentioning

confidence: 99%

A Pilot Study on Duodenal Acid Exposure and Its Relationship to Symptoms in Functional Dyspepsia with Prominent Nausea

et al. 2004

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BACKGROUND: Duodenal hypersensitivity to acid and decreased duodenal clearance of exogenous acid have been reported in functional dyspepsia (FD). However, the relevance of these abnormalities to spontaneous duodenal acid exposure and dyspeptic symptoms in FD is unknown. AIMS:To determine spontaneous duodenal acid exposure and its relationship with symptoms, duodenal sensitivity to acid, and the effects of a 5-HT 3 receptor antagonist on duodenal responses to acid in FD. METHODS:Eleven FD patients with prominent nausea and 11 healthy controls underwent 24-h ambulatory duodenal pH monitoring with assessment of dyspeptic symptoms. On the next day, duodenal bolus infusions of 5 ml of acid and normal saline were given in a randomized double-blind manner and repeated after ondansetron or a placebo. RESULTS:Nighttime duodenal acid exposure was similar, but FD patients had lower duodenal pH and higher duodenal % time (pH < 4) than controls during the daytime and in the second postprandial 2 h (p < 0.05). Seven patients (64%) with duodenal acid exposure above the normal range had higher severity scores for several dyspeptic symptoms including nausea. However, the symptom severity was poorly or weakly correlated to duodenal pH, and brief duodenal acid infusion did not affect any symptoms. Duodenal responses to exogenous acid were unaffected by 5-HT 3 receptor antagonism.CONCLUSIONS: Spontaneous duodenal acid exposure is increased in a subset of FD patients with prominent nausea, and this is associated with more severe dyspeptic symptoms. However, a direct relationship between duodenal acid exposure and symptom severity is lacking.

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“…A fourth group of patients do not fall into any subgroup and are classified as unspecified (6). There has been support for the role of acid in the etiology of NUD even though the basal and peak acid secretion have been shown to be normal (7). The results of studies with acid suppressants have been conflicting (2,8,9) whereas studies with antacids have been universally negative (8)(9)(10)(11).…”

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confidence: 99%

A Double‐Blind Randomized Study of Cisapride in the Treatment of Nonulcer Dyspepsia

MacCANNELL

Thomson

et al. 1997

Canadian Journal of Gastroenterology and Hepatology

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MC CHAMPION, KL MACCANNELL, ABR THOMSON, ET AL, FOR THE CANADIAN CISAPRIDE NUD STUDY GROUP.A double-blind randomized study of cisapride in the treatment of nonulcer dyspepsia. Can J Gastroenterol 1997;11(2):127-134. Cisapride is a substituted benzamide with gastrointestinal prokinetic effects presumed to be due to the enhancement of the physiological release of acetylcholine at the myenteric plexus. In a multicentre study, 189 patients with nonulcer dyspepsia (NUD) received single-blind placebo treatment for two weeks. A total of 123 patients with no or minimal response to placebo and epigastric pain of at least moderate severity and frequency were randomly assigned to one of three parallel double-blind treatments for six weeks: cisapride 10 mg tid, cisapride 20 mg tid or placebo. The severity and frequency of individual symptoms (epigastric pain, heartburn, nausea, vomiting, anorexia, postprandial discomfort, regurgitation, lower abdominal pain, bloating and constipation) were assessed on a four-and five-point categorical scale, respectively, by the investigator at three on-treatment visits and by patients in a daily diary. Analysis of investigator and patient assessments for differences in symptom severity x frequency composite scores among the three treatment groups showed no statistically significant differences for individual symptoms or symptom clusters. As assessed by the investigator, and compared with baseline, cisapride 20 mg tid significantly (P<0.05) improved epigastric pain, bloating and early satiety as well as improved the total symptom cluster. Investigator evaluation of the five most severe and frequent symptoms for each patient showed statistically significant improvement in each treatment group. For patient diary assessments, statistically significant within-treatment improvement of the total symptom cluster, the five most severe symptoms cluster, bloating and early satiety was observed for both cisapride 20 mg and placebo, whereas epigastric pain significantly (P<0.05) improved in all three treatment groups. Investigator evaluation of global response (good + excellent) rate at the end of the six-week treatment period was 38% for cisapride 20 mg, 47% for cisapride 10 mg and 33% for placebo. No statistically significant difference in this parameter among treatments was noted. Cisapride was well tolerated at both doses with a side effect profile comparable with that of placebo. It is concluded that, in this double-blind multicentre study with a single-blind two-week placebo run-in phase, cisapride 10 mg tid and 20 mg tid were not effective compared with placebo in improving symptoms in NUD patients. This study re-emphasizes the good prognosis of patients with NUD, with 14% of patients improving in the two-week placebo run-in phase and a further 33% improving in the next six weeks while on placebo. Within-treatment analysis of investigator assessments showed improvement for cisapride 20 mg tid suggesting a trend for efficacy at this dose. (Pour le résumé, voir page 128) Key Words: Cisapride, N...

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Basal gastric acid secretion in nonulcer dyspepsia with or without duodenitis

Cited by 73 publications

References 13 publications

Targeting the Abnormalities of Gastroduodenal Functions in Functional Dyspepsia

Targeting the Abnormalities of Gastroduodenal Functions in Functional Dyspepsia

A Pilot Study on Duodenal Acid Exposure and Its Relationship to Symptoms in Functional Dyspepsia with Prominent Nausea

A Double‐Blind Randomized Study of Cisapride in the Treatment of Nonulcer Dyspepsia

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